尼麦角林对偏头痛患者脑血流动力学与血浆5-羟色胺的影响

目的探讨尼麦角林对偏头痛患者脑血流动力学与血浆5-羟色胺(5-HT)水平的影响。方法选择67例偏头痛患者随机分为尼麦角林治疗组(35例)和对照组(32例),同时选择30例健康体检者为健康对照组,治疗组应用尼麦角林治疗,对照组应用双氯芬酸钠治疗,应用经颅多普勒超声(TCD)技术检测治疗组和对照组治疗前后及健康对照组双侧大脑中动脉、大脑前动脉、椎动脉和基底动脉的(mean velocity,Vm)变化。采用高效液相色谱紫外光法测定3组血浆5-HT浓度,比较3组颅内动脉血流动力学的改变与血浆5-HT水平。结果 67例服药前大脑前动脉、大脑中动脉、椎动脉和基底动脉的平均血流速度与健康对照组比较增快。治疗后对照组变化不明显,治疗组大脑前动脉、大脑中动脉、椎动脉和基底动脉的平均血流速度降低,且与健康对照组比较差异无统计学意义(P0.05)。与健康对照组比较,偏头痛患者(治疗组和对照组)发作期血浆5-HT水平降低,发作间期血浆5-HT水平升高,差异有统计学意义(P0.05)。治疗后治疗组血浆5-HT水平发作期较治疗前和对照组显著升高,发作间期较治疗前和对照组明显下降(P0.05)。结论尼麦角林可明显预防和减轻偏头痛患者的发作,改善偏头痛患者的脑血流,调节偏头痛患者发作期和发作间期的血浆5-HT水平可能是其作用机制之一。     

天麻素联合尼麦角林治疗眩晕症的疗效分析

目的：探讨天麻素联合尼麦角林治疗眩晕症的临床疗效。方法36例眩晕症患者随机分为2组，每组各18例。对照组给予尼麦角林治疗，观察组在对照组的基础上联合使用天麻素治疗。疗程结束后比较疗效、眩晕评分、主要症状消失时间及不良反应。结果观察组总有效率100.0％，明显高于对照组的66.7％（ P＜0.05）。治疗前2组眩晕评分比较无明显差异（ P＞0.05），治疗后观察组眩晕评分由（2.28±1.17）分增高至（4.37±0.73）分，对照组由（2.32±1.04）分增高至（3.72±0.89）分，观察组治疗后评分明显高于对照组，差异有统计学意义（ P＜0.05）。观察组眩晕、耳蜗综合征、植物神经症状及前庭功能受损消失时间均明显短于对照组，差异有统计学意义（ P均＜0.05）。2组均未出现严重的不良反应，药物安全性好。结论天麻素联合尼麦角林治疗眩晕症疗效可靠，可提高治疗有效率，增加眩晕评分，缩短主要症状消失时间，且不良反应少，值得临床推广。     

尼麦角林对放射性脑损伤患者脑功能重塑的临床研究

目的 探讨尼麦角林对因头颈部肿瘤采取放疗治疗致放射性脑损伤患者脑功能重塑的影响.方法 回顾性分析我院与三九脑科医院2010-01-2014-01收治的84例放射治疗致脑损伤的患者的临床资料,随机分为观察组和对照组各42例,对照组行常规康复治疗,观察组在对照组基础上加用尼麦角林.比较2组康复治疗前及康复治疗后第2周、4周相关神经功评分及治疗4周后头痛症状、MRI病灶变化分级等指标差异.结果 观察组神经功能缺损程度评分、ADL、MESSS评分改善均显著优于对照组,差异均有统计学意义(P＜0.05).观察组头痛症状分布和总有效率显著优于对照组,差异均具有统计学意义(P＜0.05),头颅MRI病灶变化显效率及总有效率均显著高于对照组,差异均有统计学意义(P＜0.05).结论 尼麦角林对于放射性脑损伤脑功能重建有积极作用,值得临床应用推广.     

尼麦角林对轻度认知损伤患者的干预治疗分析

目的 采用尼麦角林对轻度认知损伤(MCI)患者进行治疗,观察其服药后的认知功能的变化.方法 入选31例MCI患者,尼麦角林组16例,口服尼麦角林10mg,3次/d,连续用药3个月,对照组15例,用药前后均行认知功能评定.结果 与对照组相比,尼麦角林组用药后词语即刻回忆,符号数字转换以及简易智力状态测查的成绩显著提高(P＜0.05).结论 服用尼麦角林对MCI患者的记忆力、注意力有一定改善,进而使MCI患者总体认知功能也有提高.     

低频rTMS治疗以疼痛症状为主的焦虑患者疗效观察

目的：探讨低频重复经颅磁刺激（低频rTMS）对以疼痛症状为主焦虑患者的治疗作用。方法68例以疼痛症状为主焦虑患者随机分为2组,对照组33例,口服常规抗焦虑药物;治疗组35例,在口服抗焦虑药物的同时,加用低频重复经颅磁刺激治疗,疗程4周,以汉密尔顿焦虑量表（HAMA）、疼痛视觉模拟评分（VAS）对患者的焦虑程度、疼痛程度及改善状况进行评定,并将2组疗效作对比。结果2组治疗前后 HAMA评分和VAS评分对比,差异均有统计学意义（P＜0.05）,组间比较差异有统计学意义（ P＜0.05）;总有效率治疗组94.29％,对照组81.82％,差异有统计学意义（ P＜0.05）。结论低频重复经颅磁刺激（低频rTMS）治疗以疼痛症状为主的焦虑患者安全有效。     

尼麦角林联合盐酸多奈哌齐治疗血管性痴呆的临床疗效观察

目的研究血管性痴呆患者采用尼麦角林联合盐酸多奈哌齐的治疗效果。方法抽取2014-03—2015-06在我院治疗的60例血管性痴呆进行分组研究,随机分为观察组与对照组各30例,对照组服用尼麦角林,观察组联合服用尼麦角林及盐酸多奈哌齐,对比观察2组患者治疗效果及日常生活能力量表评分(ADL)、简易智能状态检查量表评分(MMSE)和不良反应。结果观察组治疗总有效率80.00%,对照组56.67%,差异有统计学意义(P0.05);治疗前观察组与对照组ADL及MMSE评分对比,差异无统计学意义(P0.05);经治疗后,观察组ADL评分明显低于对照组,MMSE评分均明显高于对照组,差异有统计学意义(P0.05);2组患者均未出现不良反应。结论采用尼麦角林联合盐酸多奈哌齐治疗血管性痴呆患者疗效确切,治疗有效率较高,安全性较高,能够显著改善患者认知功能和日常生活能力,对提高患者生活质量具有重要意义,值得推广运用。     

尼麦角林治疗脑梗死伴认知功能障碍的疗效观察

目的 观察尼麦角林治疗脑梗死伴认知功能障碍的疗效.方法 对60例伴有认知功能障碍的脑梗死患者随机分为治疗组和对照组,在常规药物治疗的基础上,治疗组加用尼麦角林片,3次/d,每次口服10mg,连用3个月.在治疗前和治疗后3个月,采用简易智力状态检查量表(MMSE)、中国脑卒中临床神经功能缺损程度评分量表(CSS)、巴氏指数(BI)评定患者的功能.结果 治疗组患者的认知功能改善明显优于对照组(P＜0.01).结论 尼麦角林能改善脑梗死患者的认知功能.     

托吡酯联合舍曲林治疗双相抑郁急性发作的对照研究

目的 评价与拉莫三嗪联合舍曲林治疗双相抑郁急性发作相比,托吡酯联合舍曲林治疗双相抑郁的疗效及安全性.方法 将符合CCMD -3双相抑郁诊断标准的68例患者随机进入拉莫三嗪联合舍曲林组(研究组)或托吡酯联合舍曲林组(对照组)接受治疗,最终研究组有30例和对照组有34例完成治疗,分别在治疗前和1、2、4、6、8周末评定HAMD、HAMA、TESS总分.结果 两组间HAMD、HAMA评分在第4、6周末具有统计学意义(P＜0.01,P＜0.05).两组内各阶段末HAMD、HAMA评分具有统计学意义(P＜0.01),提示托吡酯联合组与拉莫三嗪联合组对双相抑郁急性发作有效.两组TESS不良反应在第2、4周末差异具有统计学意义(P＜0.01).结论 托吡酯联合舍曲林治疗双相抑郁在疗效方面,有效且起效时间快;在安全性方面,托吡酯联合舍曲林治疗双相抑郁时不良反应较早出现,但经过持续坚持观察治疗后,在不良反应方面与拉莫三嗪联合舍曲林治疗双相抑郁的不良反应相当.     

帕罗西汀联合西比灵预防更年期偏头痛的临床分析

目的 探讨帕罗西汀联合西比灵对更年期偏头痛发作的预防作用.方法 将80例更年期偏头痛患者随机分成2组,帕罗西汀联合西比灵为治疗组,单用西比灵为对照组,观察治疗前后偏头痛发作次数、持续时间,同时采用汉密尔顿抑郁量表(HAMD)和汉密尔顿焦虑量表(HAMA)进行评定.结果 上述两项头痛指标在2组治疗前后均有统计学意义,治疗前后组间比较偏头痛发作次数有统计学意义(P＜0.05);治疗组尚能明显减轻患者抑郁焦虑症状.结论 帕罗西汀联合西比灵对预防更年期偏头痛发作优于单用西比灵.     

黛力新联合西比灵治疗偏头痛伴抑郁和焦虑90例疗效观察

目的观察黛力新联合西比灵治疗偏头痛伴焦虑、抑郁情绪患者的疗效与不良反应。方法将90例伴抑郁和焦虑的偏头痛患者随机均分为2组,治疗组给予黛力新与西比灵口服,对照组单用西比灵,均以6周为1个疗程。根据治疗前后头痛发作次数、持续时间及头痛严重程度的变化进行疗效评定,并用汉密尔顿抑郁量表（HAMD）和汉密尔顿焦虑量表（HAMA）进行评分,自制副反应量表记录不良反应。结果两种治疗方法均可显著减少偏头痛发作次数,缩短头痛发作时间,减轻头痛程度（P〈0.05）;治疗组还可明显减轻患者的抑郁、焦虑症状,治疗后2、4、6周HAMD和HAMA评分的改善优于对照组（P〈0.01）;治疗组头痛持续时间缩短也优于对照组（P〈0.05）。结论黛力新联合西比灵治疗伴情绪障碍的偏头痛疗效较好,不良反应不需作特殊处理。     

Diagnostic Difficulties and Treatment Implications

Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.     

Cognitive Dysfunction Associated with Antiepileptic Drug Therapy

Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.     

Carbamazepine Efficacy in Adults With Partial and Generalized Tonic-Clonic Seizures

Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.     

Etiologic and Preventive Aspects of Epilepsy in the Child–Bridging the Gap Between Laboratory and Clinic

Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.     

Predisposing and Causative Factors in Childhood Epilepsy

Summary: We review information from large studies of defined populations, examining the role of known factors and especially of prenatal and perinatal factors in contributing to nonfebrile seizure disorders of early childhood. We depend especially, but not exclusively, on the recently completed analyses from the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, the NCPP. About 4% of children in the NCPP who had at least one non-febrile nonsymptomatic seizure by the age of 7 years had a previous seizure during acute neurologic illness, such as meningitis or during the acute illness after trauma. Many such seizures should potentially be preventable. Of children with seizures, 10% had had a neonatal seizure and 13% had had a febrile seizure. Among the hundreds of prenatal and perinatal factors explored as predictors of childhood seizure disorders, the principal predictors identified were congenital malformations of the fetus, cerebral and noncerebral; family history of certain neurologic disorders; and neonatal seizures. In agreement with the British National Child Development Study, labor and delivery factors in the NCPP appeared to contribute very little to childhood seizure disorders. Maldevelopment, rather than damage at birth to an initially intact nervous system, appeared to be the more common mechanism. Most seizure disorders of early childhood remained unexplained by the large set of prenatal and perinatal characteristics examined.     

Anticonvulsant Drugs and Cognitive Function: A Review of the Literature

Summary: Alterations of cognitive function are separate from disturbances of behavior seen in association with epilepsy. The nature of the cognitive disability may to a certain extent depend on the seizure type. Partial seizures, mainly derived from a temporal lobe focus, impair memory tasks, while generalized seizures seem to have more effect on attentional abilities. A number of studies, reviewed in this paper, suggest that anticonvulsant drugs further impair cognitive function. Maximal impairments are seen in patients receiving polytherapy: rationalization of polytherapy improves cognitive abilities. Studies in children and adults have allowed differentiation of the effects of various commonly used antiepileptic agents. Maximal cognitive deficits are seen with. phenytoin, while phenobarbital and sodium valproate induce moderate disturbances, and carbamazepine seems relatively free from such toxicity. Further research is needed on the interrelationship between types of seizure disorders, types of anticonvulsant medications, and cognitive function.     

Effects of NMD A- and AMPA-Receptor Antagonists on Different Forms of Epileptiform Activity in Rat Temporal Cortex Slices

Summary: Lowering extracellular magnesium induces different patterns of epileptiform activity in rat hippocampus and entorhinal cortex. Short recurrent epileptiform discharges in the hippocampus are stable over time, whereas seizurelike events (SLEs) in the entorhinal cortex, the subiculum, and the neighboring neocortex develop into late recurrent discharges which are not blocked by clinically employed antiepileptic drugs. We tested the sensitivity of the different epileptiform discharge patterns to. /V-methyl-D-aspartate (NMDA)- and non-NMDA-receptor antagonists. As NMDA-receptor antagonist we used dextrorphan, ket-amine, and 2-aminophosphonovalerate (2APV); as α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)-receptor antagonist we employed the quinoxaline derivative glutamate 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The findings show that the different patterns of epileptiform activity, including the late recurrent discharges, are sensitive to all NMDA-receptor antagonists. However, when dextrorphan was employed to suppress seizure-like events, later recurrent discharges did not develop during the remaining time course of the experiment. CNQX reversibly suppressed recurrent discharges in the hippocampus and SLEs in the entorhinal cortex. However, late recurrent discharges become insensitive to CNQX, even at a high concentration of 60 μM m. This finding suggests a prominent role for NMDA receptors in the generation of late recurrent discharges.     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.     

The influence of comorbid depression on seizure severity

PURPOSE: To determine the relation between depressive symptoms and seizure severity among people with epilepsy. METHODS: A postal questionnaire was used to survey a nationwide community sample about seizures and depression. The Seizure Severity Questionnaire (SSQ) assessed the severity and bothersomeness of seizure components. The Centers for Epidemiological Studies-Depression scale categorized levels of depression. RESULTS: Respondents categorized as having current severe (SEV, n = 166), mild-moderate (MOD, n = 74), or no depression (NO, n = 443) differed significantly in SSQ scores (all p < 0.0001). People with SEV or MOD reported significantly worse problems than did those with NO depression for overall seizure recovery (mean, 5.3, 4.9, 4.5, respectively); overall severity (5.0, 4.5, 4.2); and overall seizure bother (5.3, 4.8, 4.4) (all p < 0.005). Cognitive, emotional, and physical aspects of seizure recovery also were rated worse among people with SEV than with NO depression (all p < 0.05). Symptoms of depression were significantly correlated with higher levels of all components of generalized tonic-clonic seizure severity (r = 0.33-0.48; all p < 0.0001), and partial seizures (r = 0.31-0.38; all p < 0.01). CONCLUSIONS: Clinically depressed people with epilepsy reported higher levels of perceived severity and bother from seizures, as well as greater problems with overall seizure recovery than did nondepressed people experiencing similar types of seizures. The pervasive influence of depressive symptoms on reports of seizure activity suggests that people with epilepsy should be screened for depression. These data highlight the importance of detecting and treating depression among people with epilepsy.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.